title: Relative roles of the cellular and humoral responses in the Drosophila host defense against three gram-positive bacterial infections.
abstract: BACKGROUND
  Two NF-kappaB signaling pathways, Toll and immune deficiency (imd), are required for survival to bacterial infections in Drosophila. In response to septic injury, these pathways mediate rapid transcriptional activation of distinct sets of effector molecules, including antimicrobial peptides, which are important components of a humoral defense response. However, it is less clear to what extent macrophage-like hemocytes contribute to host defense.
  
  
  RESULTS
  In order to dissect the relative importance of humoral and cellular defenses after septic injury with three different gram-positive bacteria (Micrococcus luteus, Enterococcus faecalis, Staphylococcus aureus), we used latex bead pre-injection to ablate macrophage function in flies wildtype or mutant for various Toll and imd pathway components. We found that in all three infection models a compromised phagocytic system impaired fly survival--independently of concomitant Toll or imd pathway activation. Our data failed to confirm a role of the PGRP-SA and GNBP1 Pattern Recognition Receptors for phagocytosis of S. aureus. The Drosophila scavenger receptor Eater mediates the phagocytosis by hemocytes or S2 cells of E. faecalis and S. aureus, but not of M. luteus. In the case of M. luteus and E. faecalis, but not S. aureus, decreased survival due to defective phagocytosis could be compensated for by genetically enhancing the humoral immune response.
  
  
  CONCLUSIONS
  Our results underscore the fundamental importance of both cellular and humoral mechanisms in Drosophila immunity and shed light on the balance between these two arms of host defense depending on the invading pathogen.
authors.affiliation: Equipe Fondation Recherche Médicale, UPR 9022 du Centre National de la Recherche Scientifique, Institut de Biologie Moléculaire et Cellulaire du CNRS, Université de Strasbourg, Strasbourg, France.
authors.forename: Nadine T
authors.initials: NT
authors.lastname: Nehme
authors.forename: Jessica
authors.initials: J
authors.lastname: Quintin
authors.forename: Ju Hyun
authors.initials: JH
authors.lastname: Cho
authors.forename: Janice
authors.initials: J
authors.lastname: Lee
authors.forename: Marie-Céline
authors.initials: MC
authors.lastname: Lafarge
authors.forename: Christine
authors.initials: C
authors.lastname: Kocks
authors.forename: Dominique
authors.initials: D
authors.lastname: Ferrandon
mesh_terms: D000818:Animals; D023181:Antimicrobial Cationic Peptides / Q000276:immunology / Q000494:pharmacology; D002352:Carrier Proteins / Q000378:metabolism; D029721:Drosophila Proteins / Q000378:metabolism; D004331:Drosophila melanogaster / Q000166:cytology / Q000187:drug effects / Q000276:immunology* / Q000382:microbiology*; D013293:Enterococcus faecalis / Q000187:drug effects / Q000276:immunology; D006094:Gram-Positive Bacteria / Q000187:drug effects / Q000276:immunology*; D016908:Gram-Positive Bacterial Infections / Q000276:immunology* / Q000382:microbiology; D054884:Host-Pathogen Interactions / Q000187:drug effects / Q000276:immunology*; D007111:Immunity, Cellular / Q000187:drug effects / Q000276:immunology*; D056724:Immunity, Humoral / Q000187:drug effects / Q000276:immunology*; D007113:Immunity, Innate / Q000187:drug effects; D016982:Micrococcus luteus / Q000187:drug effects / Q000276:immunology; D009895:Opsonin Proteins / Q000378:metabolism; D010587:Phagocytosis / Q000187:drug effects / Q000276:immunology; D011956:Receptors, Cell Surface / Q000378:metabolism; D015398:Signal Transduction / Q000187:drug effects; D012995:Solubility / Q000187:drug effects; D013211:Staphylococcus aureus / Q000187:drug effects / Q000276:immunology
chemical_list: D023181:Antimicrobial Cationic Peptides; D002352:Carrier Proteins; D029721:Drosophila Proteins; C480085:Gnbp1 protein, Drosophila; D009895:Opsonin Proteins; D011956:Receptors, Cell Surface; C505820:eater protein, Drosophila; C118897:peptidoglycan recognition protein